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Studies on estrogen induced pituitary tumor in the rat with special reference to the relationship of the tuberoinfundibular dopamine neuron system

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Abstract

Pituitary tumors were experimentally induced in female Wistar rats by repeated injections of estradiol dipropionate. The hypothalamus and pituitary tumors were studied simultaneously by fluorescence histochemistry and immunohistochemistry. The pituitary gland became larger with a concomitant increase of serum prolactin in proportion to the dose of estrogen. Estrogen-induced pituitary tumor exhibited a proliferating prolactin cells by the peroxidase immunohistochemical method. Ultramicroscopical findings showed that these tumor cells were in an extremely hyperfunctional state.

The dopamine neuronal perikarya in the hypothalamic arcuate nucleus and their terminals in the external layer of the median eminence were examined by fluorescence histochemistry in the rats bearing estrogen induced pituitary tumor and it was concluded that in our experimental conditions, estrogen effected directly on pituitary rather than on the hypothalamus and consequently dopamine synthesis in the arcuate neurons and its release into portal capillaries were accerelated simultaneously in order to inhibit prolactin secretion from tumor cells.

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Authors and Affiliations

  1. Department of Neurosurgery, Kyoto Prefectural University of Medicine, Kawaramachi Hirokoji, Kamigyoku, 602, Kyoto, Japan

    Masahito Fujimoto, Eiji Yoshino & Kimiyoshi Hirakawa

  2. Department of Anatomy, Kyoto Prefectural University of Medicine, Kawaramachi Hirokoji, Kamigyoku, 602, Kyoto, Japan

    Yasuhiko Ibata

  3. Third Division, Department of Medicine, Kobe University, School of Medicine, Kobe, Japan

    Kazuo Chihara

Authors
  1. Masahito Fujimoto
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  2. Eiji Yoshino
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  3. Kimiyoshi Hirakawa
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  4. Kazuo Chihara
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  5. Yasuhiko Ibata
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Fujimoto, M., Yoshino, E., Hirakawa, K. et al. Studies on estrogen induced pituitary tumor in the rat with special reference to the relationship of the tuberoinfundibular dopamine neuron system. J Neuro-Oncol 5, 151–159 (1987). https://doi.org/10.1007/BF02571303

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